Liliana Torosantucci

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: This work reports a new interaction between PINK1 and Beclin1, a key pro-autophagic protein already implicated in the pathogenesis of Alzheimer's and Huntington's diseases, and identifies a new function of Pink1 and further strengthen the link between autophagy and proteins implicated inThe neurodegenerative process.

TL;DR: It is shown that, following mitophagic stimuli, autophagosomes also form at MAM; moreover, endogenous PINK1 and BECN1 were both found to relocalize at M AM, where they promoted the enhancement of ER-mitochondria contact sites and the formation of omegasomes, that represent autophagy precursors.

TL;DR: It is reported that, upon mitochondrial depolarization, PINK1 interacts with and phosphorylates Bcl-xL, an anti-apoptotic protein also known to inhibit autophagy through its binding to Beclin-1, suggesting a novel mechanism through which Pink1 regulates cell survival.